Thursday, April 30, 2015

A woman in late middle age with a history of a mild stenosis of the RCA seen on CT coronary angiogram 4 years prior presented 2 hours after the onset of nondescript substernal chest discomfort that radiated to both axillae.

Her daughter was worried and brought her to the ED. This is her initial ECG:

There is a suggestion of inferior MI: the T-waves in II, III, and aVF are slightly large. There is T-wave inversion in aVL, which is a soft sign of inferior MI.

She received nitroglycerin, and the discomfort was relieved, but she attributed the relief to the removal of a tight-fitting garment.

A repeat ECG was unchanged after pain relief.

I was worried about her, but with pain resolution and a non-diagnostic ECG, there was no indication for cath lab activation at night.

The first troponin was undetectable.

Nevertheless, I was still worried about her and gave her aspirin, ticagrelor, and heparin, and admitted her to the hospital.

After admission, serial troponin I later climbed, peaking at 1.6 ng/mL.

A formal Echo the next AM showed an inferior wall motion abnormality. A repeat ECG in the morning was recorded:

This shows resolution of the enlarged T-waves, confirming that there had been inferior ischemia.

I was sure there would be a tight RCA lesion that would need stenting.

However, the angiogram showed a chronic total occlusion of the RCA, with the inferior wall supplied by collaterals. No stent was deployed.

The angiographer explained it this way: "she could have had some small left to right collateral channels that closed off, and then she recruited more collaterals to reperfuse." Perhaps as a result of nitroglycerin.

Nevertheless, until angiography was done, this was presumed ACS of the RCA (or possibly circumflex) until proven otherwise.

Learning Point

1. Inferior hyperacute T-waves can be extremely subtle

2. Even if they do not lead you to cath lab activation, such T-waves, along with lead aVL and the convincing history, may persuade you in spite of an undetectable troponin, to give maximal medical therapy (aspirin, ticagrelor, and heparin) for ACS.

3. The territory of a chronic total occlusion which is supplied by collaterals is particularly vulnerable.

Monday, April 27, 2015

A middle aged male with some coronary risk factors presented to the ED after an episode of typical sounding chest pain that was resolved upon arrival.

He was in the ED for an hour when he developed chest pain again and had this ECG immediately recorded:

There is sinus rhythm at a rate of about 60. There is ST elevation at the J-point that does not quite meet "STE criteria" of 2 mm for these 2 leads. There is no convexity, ST depression, or Q-waves that would tell us that this ST elevation is clearly pathologic. So we can use the formula that differentiates STE from LAD occlusion from that due to early repolarization (normal variant). The computerized QTc = 400, STE60V3 = 2.5, RV4 = 19; so the formula value = 20.39, and this is consistent with normal ST elevation.

So the ECG is normal, right?

Some Background

What I neglected to tell you is that when the patient had arrived pain free, he had this ECG recorded:

Here there is subtle terminal T-wave inversion in V2, and a bit in V3, typical of early Pattern A Wellens' waves.

It triggered the recording of serial ECGs (sorry, not available) which showed increasing ST elevation diagnostic of LAD occlusion.

So this was Wellens' syndrome, a state of spontaneous reperfusion of the LAD, manifesting with "reperfusion T-waves" and R-wave preservation after an episode of closure of the LAD. Thus, the patient presents pain free after an episode of angina.

The importance of Wellens' syndrome is that the artery can close off again at any moment, in which case the inverted T-waves will become upright again and look normal. This is called "pseudonormalization".

The first ECG was recorded so soon after re-occlusion of the artery that this ECG shows no signs of occlusion other than pseudonormalization, which requires comparison with the previous.

This is my most popular lecture, which Scott Joing of www.hqmeded.com just recorded for me in his amazing video recording studio.

When I give this lecture real-time, I usually do it in a workshop and have more time - enough time to stop and let people get a good look at the ECG and try to find the critical elements for themselves before going on to explain them. That makes for a significantly longer lecture.

But if you want to have time to scrutinize any ECG, just pause the video to look at the ECG for a while before you play my explanation.

Troponins were minimally elevated, consistent with type 2 MI from low flow state of cardiac arrest and high demand state of atrial fib with RVR.

The patient underwent angiography later (the next day) and there was no culprit lesion. He did not have ACS.

He recovered and had an ICD implanted.

Learning Points:

1. Ventricular fibrillation is not only caused by acute coronary syndrome. There are many other etiologies, including scarring from previous MI, medications, drugs, LVH, and channelopathies. We found that 38% of out of hospital ventricular fibrillation was due to STEMI. The remainder were due to other etiologies, (including NonSTEMI ACS). But approximately 50% were due to non-ACS etiologies.

2. ST depression (with reciprocal ST elevation in lead aVR) is common shortly after BOTH resuscitation from ventricular fibrillation AND after cardioversion from atrial fibrillation.

3. One should wait a short time (15 minutes?) to record another 12-lead ECG to ascertain whether there is ongoing ischemia and probable ACS, or whether the ST depression is transient only.

4. Not all patients with ventricular fibrillation necessarily need emergent angiography. Much depends on the post resuscitation ECG and its evolution shortly after defibrillation.

Tuesday, April 21, 2015

A middle-aged male complained of acute onset of chest pain. He was diaphoretic, weak, lightheaded, but alert. Blood pressure was 60/palp with a pulse of 40. was given aspirin and a 500 ml normal saline bolus.

Here is the prehospital 12-lead:

There is bradycardia and some kind of AV block. P-waves are difficult to discern, so the exact nature of the block is unclear

There is obvious inferior STE. Reciprocal ST depression in aVL confirms inferior STEMI, and ST depression in lead I is a good indicator that this is an RCA occlusion.

In inferior MI due to RCA occlusion, one should always look to lead V1 for ST elevation indicating right ventricular infarct also.

Here, there is ST depression in V1 and V2, but ST elevation in V3. This is odd and one must suspect that leads V1 and V3 are reversed.

The ST depression in V2 shows extension to the posterior wall.

The cath lab was activated by the medics.

The patient arrived alert and conversant. BP was in the 40's to 60's, with pulse in 30s to 40s.

An ECG was recorded 11 minutes after the first:

Now it is clearly 3rd degree AV block.There is clearly ST elevation in V1 (and now also V2) confirming right ventricular involvement, and confirming that prehospital leads were reversed. This is such a large RV infarct that the ST elevation extends all the way to V3, which is often called a "Pseudoanteroseptal MI" (See more cases of pseudoanteroseptal MI)

A right sided ECG was immediately recorded (limb leads are not changed):

3rd degree heart block. There is ST elevation in V2R (identical to V1 on regular 12-lead) extending all the way out to V6R

A bedside echo was done:

There is bradycardia. The RV is massively dilated due to RV failure from RV infarct.

He was given ticagrelor and heparin. He was given 25 mg of ketamine and transcutaneous pacing was begun. Capture was achieved at 114 mA at a rate of 70. Systolic BP rose to 110.

Capture was verified by bedside echo:

He went for angiogram which showed occlusion of the proximal RCA, proximal to the right ventricular marginal branch to the RV.

It was opened and stented.

The patient did well.

Learning Points

1. Occlusion of the proximal RCA may result in hemodynamically significant RV MI.
2. These occlusions also frequently lead to complete AV block because of blood supply to the AV node from the RCA
3. RV MI can lead to RV failure and dilatation
4. Fluids are indicated, as cardiogenic shock due to RV failure responds to fluid loading and does NOT result in pulmonary edema
5. Transcutaneous pacing can be verified with bedside ultrasound.
6. Rapid reperfusion of RV MI results in a good outcome

Sunday, April 19, 2015

An elderly person collapsed and was found to be pulseless. He had immediate bystander CPR. An AED was placed and one shock was given within 5 minutes of arrest. He immediately awoke. EMS arrived and recorded these ECGs:

He was stable en route to the ED. On arrival, he was awake and complained of only mild aching left chest pain. He stated that prior to his collapse, he had been walking briskly and was feeling short of breath, but not having any chest pain. He does have a history of CAD with a stent, and takes clopidogrel, but he did not take it on this particular day.

He had this ED ECG recorded, 13 min after first

There is inferior ST elevation with reciprocal ST depression in aVL, diagnostic of inferior injury. The hyperacute T-waves in V4-V6 are diminished and there is less ST elevation.

The cath lab was activated. He was given aspirin and heparin.

Prior to transport, another ECG was recorded. This one is 25 min after first prehospital, and 12 min after the first ED ECG:

There is nearly complete resolution of all injury pattern

Angiogram showed no culprit, but did show severe 3 vessel disease, with 100% chronic LAD and RCA occlusions, and chronic 75% circumflex. All territories were supplied by collaterals from the circumflex!

Wednesday, April 15, 2015

This is another contribution from Victoria Stephen. Victoria is a third year EM Registrar from at the University of the Witwatersrand in Johannesburg, South Africa, and a great asset to FOAMed. Follow her on Twitter: @EMcardiac.

A 91 year old presented to the ED of a small hospital with a history of
sudden onset syncope. A family member thought she was having a seizure.
She reported no chest pain or dyspnoea when conscious. The patient had a
history of hypertension which was poorly controlled.

She appeared alert and well-oriented. Her initial BP was 184/90, HR 41 BPM. An ECG was recorded in the ED:

There is second degree heart block with a HR of 41 BPM. The QRS complex is 144ms indicating an infranodal escape. There is an RBBB configuration with a LAFB, indicating it may be originate from the left posterior hemi-fascicle. The QTc is significantly prolonged at 535 ms. There are deep wide bizarre looking T waves seen in virtually all the leads, but most notably in the precordial leads.

She had a
CT of the Brain which showed no intracranial bleed. Her renal function was
normal and the electrolytes including calcium and magnesium were normal.
Two troponin I were increased at 140 ng/L (0.14 ng/mL) and 70 ng/L (0.070 ng/mL) on consecutive
days, (negative is less than 40 ng/L for this assay).

Two days later she was
referred to a regional hospital where she was admitted to the CCU with
the following ECG:

An
informal bedside echo done by a cardiologist showed a normal ejection
fraction with no regional wall motion abnormalities. In view of the
positive troponins and the T wave inversions she was taken to the cath
lab for angiography, as well as for a pacemaker. No obstructive coronary
artery disease was present. She subsequently developed runs of VT while
in the lab which were too transient to determine the specific type of VT. A transvenous pacing wire was inserted for temporary pacing and the
decision was made to bring her back for a permanent pacemaker.

Here is the ECG post venous pacemaker:

Notice the T-wave inversion is present in spite of the ventricular pacing, which should result in discordant T-waves (opposite the QRS). Concordant T-waves of this dimension indicate ischemia that cannot be hidden by pacing.

And here is the ECG post permanent pacemaker, recorded 7 days after the first ECG:

This is a single chamber pacemaker. HR 62 BPM. The T waves are upright in in the inferior leads and biphasic in the precordial leads.

Commentary

This
patient suffered a Stokes-Adams attack, which is a sudden loss of
consciousness due to a high grade atrioventricular block. Seizure like
activity is commonly seen in this form of syncope. Two very different
arrhythmogenic mechanisms have been shown to induce the abrupt loss of
cardiac output causing the syncope. At the onset of complete heart
block, asystole can occur for a brief period before a new pacemaker has
kicked in. Either 1) the AV node may act as the new pacemaker, leading to a
junctional or narrow escape on the ECG, or 2) infranodal tissue will take
over the pacemaker role.

The second arrhythmia
which can abruptly occur during complete heart block (CHB) is Torsade de
Pointes (TdP). TdP is an example of a triggered dysrhythmia. Triggered
dysrhythmias are heart rate dependent and are either triggered by a fast
or slow heart rate. TdP is triggered by slow heart rates. (This is why overdrive pacing to a higher rate works in terminating TdP) In some
patients, at the onset of complete heart block, there is an abrupt
decrease in heart rate as well as prolongation of the QTc. The
resulting pause plus a well-timed PVC then triggers the onset of TdP. Both asystole and TdP
following CHB are often brief, allowing the patient to
regain consciousness.

The giant inverted T waves
are not common in CHB, but are commonly seen in CHB
complicated by Stokes-Adams attacks. Their presence is not fully
understood but has been associated with TdP and stress cardiomyopathy
occurring after the onset of Complete Heart Block. Stress cardiomyopathy
is a spectrum disorder characterized by transient left ventricular
systolic dysfunction clinically, ST elevation or T wave inversions on
the ECG, and regional wall motion abnormalities on echo which are
induced by a catecholamine surge. Takotsubo cardiomyopathy is a specific
form of stress cardiomyopathy. This paper demonstrates takotsubo
cardiomyopathy developing in patients with complete heart block,
preceding TdP:

Friday, April 10, 2015

This case was submitted by my friend Dr. Victoria Stephens. She is a third year Emergency Medicine Registrar from at
the University of the Witwatersrand in Johannesburg, South Africa, and a great asset to FOAMed. Follow her on Twitter: @EMcardiac.

Case

A 71 year old man was admitted to the ICU with neutropenic sepsis
complicated by septic shock. He was intubated and ventilated and was
started on an adrenaline infusion to maintain his blood pressure. The
admission ECG was normal. Thirty-six hours into his ICU stay he went
into a cardiac arrest. The monitor showed a wide complex tachycardia.
CPR was commenced while the defibrillator was brought to the bedside. A
doctor was called from the ED to assist. The pads were attached to the
patient and the defib was placed in AED mode by the nurse. The following
rhythm strip was recorded (on a separate monitor from the AED, of course):

A rhythm strip recorded from lead II. A wide complex tachycardia is present with a rate of approximately 170 BPM. The QRS duration is very wide. It is regular and monomorphic and all but diagnostic of VT.

The
code blue team recognized that the rhythm was ventricular tachycardia
and that immediate defibrillation was required. They waited for the AED
function on the defib to recommend a shock. Instead, it kept saying
“…analysing…analysing”. No shock was advised. The doctor could not
remember how to operate the manual mode of the AED defibrillator (this was an defibrillator that has an AED mode; not all defibrillators have that). Since the AED was
not advising a shock, he assumed that the defibrillator was faulty, and called
for another defibrillator to be fetched from the ED. CPR was continued,
adrenaline and amiodarone were given. By the time the second defibrillator arrived, return of spontaneous circulation (ROSC) had occurred. The
patient converted into a normal sinus rhythm a short while later.

Comment

What happened? Why did the AED not recognize such an obvious case of VT? Was the defibrillator faulty?

No, the defibrillator was not faulty. The technology is, rather, imperfect.

How does an AED work?

The
automatic external defibrillator (AED) was initially designed to be
used by laypeople or first responders with little or no experience in
defibrillation, in order to improve survival from out-of-hospital
cardiac arrest (OHCA) (1). The AED uses a Rhythm Analysis Algorithm (RAA)
which essentially is software that is programmed to discriminate
between shockable and non-shockable rhythms. The RAA then prompts the
AED to advise or not advise a shock. The RAA uses up to 18 internal algorithms
to determine if a rhythm is shockable or not; the most
important of these are: 1) heart rate, 2) QRS width and 3) QRS amplitude.

With
regards to VT, the RAA is programmed to recognize VT as shockable only at
certain heart rates. For most AEDs, this heart rate is above 150
BPM (2). The rationale for this is twofold; 1) to prevent lay people from
potentially defibrillating a perfusing VT in a patient who may still have a pulse, and 2) that patients are more likely to arrest from VT at heart
rates greater than 150.

How does the manual defib work?

There
is no RAA. The healthcare provider decides if the rhythm is shockable
and whether a shock is advised. The number of joules for each shock is
also set by the operator.

When can the RAA in the AED fail?

Multiple
studies have demonstrated the safety and efficacy of AEDs in Cardiac
Arrest.(1) They have demonstrated not only improved survival but also
improved neurological outcomes. However, as with any device, error does
occur. The RAA in the AED can in certain circumstances fail to recognize a shockable rhythm or incorrectly advise a non-shockable rhythm to be
shocked. These circumstances are:

b. Motion artifacts caused by chest
compressions, handling of the patient, movement during ambulance
transportation, breathing and seizures may also interfere with the RAA.

Below is an example where external artifacts occurred at the beginning
of the AED analysis.(3) The AED incorrectly advised no shock for this
case of coarse VF.

This is an image of coarse VF. The AED incorrectly made a "no shock advised" decision.[Image used with permission from: Calle PA et al. Inaccurate treatment decisions of automated external
defibrillators used by emergency medical services personnel: Incidence,
cause and impact on outcome. Resuscitation 2015;88:68-74]

2) The type of shockable rhythm: they detect VF better than VT

Several
studies have examined the accuracy of the RAA by downloading the ECG
strips and responses advised from the AED memory module. (3-5) These
studies showed that the AED is more accurate in correctly detecting VF
than VT; the AED being 100% specific and 95% sensitive for coarse VF.
AEDs have also demonstrated similar accuracy in correctly detecting
non-shockable rhythms such as PEA, normal sinus rhythm, supraventricular
arrhythmias and asystole.

The
AED is much less reliable however, in correctly detecting VT: the
sensitivity for VT ranged from only 63% to 83% in these studies,
indicating that in several instances no shock was advised when VT was
actually present.

Inconsistent
shock advisories have also been demonstrated for polymorphic VT,
including the subtype Torsades de Pointes. One AED advised did not advise shock for
any of the Torsades rhythms it was subjected to(!)(2).

Several authors have recommended that manufacturers improve their
algorithms and that physicians should be aware of the potential pitfalls
in their use.

3) The VT rate

As
mentioned above, the RAA of several AEDs is set to recommend a shock if
the VT rate is more than 150. Slower forms of VT will not get a shock
advisory, even if the patient is in arrest and requires it. Though
higher VT heart rates are more likely to cause cardiac arrest,
patients with poor systolic function may not tolerate a sustained VT of
130-150 BPM and may indeed be in arrest or near-arrest. (2). Several AEDS were shown in a recent study to only advise a
shock if the VT rate exceeded 180, and others only if higher than 250 (!).(6)

In summary:

Multiple
studies have shown that the AED is very accurate at detecting VF and
tends to advise a shock nearly 100% of the time. AEDs have been shown to reduce
mortality in cardiac arrest, especially in OHCA.

The
AED is far less accurate at determining VT; with regards to both the
monomorphic and polymorphic forms. If the AED fails to recognize the VT,
the VT will eventually degrade to VF which subsequently the AED is more
likely to recognize. However, this delay may result in significant harm
to the patient’s outcome as time to defibrillation is crucial to
survival.

With
VT arrests, the trained healthcare provider is superior to the AED. For those staff who have a defibrillator with both manual and AED modes, they should know how to recognize VT, or probable VT, use the AED, and, if using the defibrillator in AED mode, know how to switch to manual mode.

Wednesday, April 8, 2015

Summary
of ED Approach to SyncopePlease excuse the formatting problems, which I have not been able to fix!I have used this to educate our residents, and I think they find it useful. It is NOT a structured review or meta-analysis.

Approach to SyncopeSyncope definition: Brief loss of consciousness with loss of postural tone and complete spontaneous recovery without medical intervention.

First: Are you sure it was syncope, and not SEIZURE? Conversely, frequently syncope has a short episode of tonic-clonic activity that mimics seizure.

--Stroke (very uncommon cause of syncope, must be TIA, as syncope implies reversibility: Subarachnoid hemorrhage (severe headache at moment of syncope), TIA
(must be either vertebrobasilar or hemispheric in patient with previous stroke of other hemisphere) Check: [History, neurological exam]

If the patient has Abdominal Pain, Chest Pain, Dyspnea or Hypoxemia, Headache, Hypotension, then these should be considered the primary chief complaint (not syncope). Most physicians will automatically be worried about these symptoms. If the patient has Abnormal Vital Signs (fever, hypotension, tachycardia, or tachypnea, or hypoxemia), then these are the primary issue to address, as there is ongoing pathology which must be identified.Also consider non-hemorrhagic volume depletion, dehydration: orthostatic vitals may uncover this [see Mendu et al. (3)].True Syncope: If, on the other hand, the patient is well, hadno other serious symptoms, has a normal sinus rhythm, and normal physical exam, then you need to be certain the syncope was not due to a dangerous brady- or tachydysrhythmia that could recur. Cardiac Syncope ("True Syncope")

a. Abnormal Electrocardiogram (ECG): Defined (San Fran syncope rule) as
any new changes when compared to the last ECG or presence of non-sinus rhythm.
If no previous ECG was available, ECG was classified as abnormal if any
abnormality was present. This San Fran definition, however, is too non-specific, so I list more specific ECG abnormalities below:b. In particular, pay attention to findings indicating these pathologies:

2. Age greater than 65 (Sarasin and STePS)3. History of Cardiovascular disease (all studies): Especially any history of heart failure or structural cardiac disease, including valvular4. Syncope without a prodrome, no precipitating factors (EGSYS)5. Hemoglobin less than 10 (SF rule)6. Syncope with Exertion (EGSYS)7. Syncope while supine (EGSYS)8. Palpitations preceding syncope (highest value on EGSYS score)9. Negative predictors of adverse outcome: Pacemaker Pre-syncope or "near-syncope" [but there is still some small risk (18)]These last two are identified in studies, but I consider them dangerous signs and symptoms in their own right, as above:10. Hypotension (obviously)11. SOB or Hypoxemia (obviously)Vasovagal (Neurocardiogenic syncope or Reflex Syncope) is the most common cause of cardiac syncope, even in patients with cardiac disease: In this entity, there is BOTH a bradycardic and/or a vasodepressor response. Thus, if there is documented sinus bradycardia, and no suspicion of high grade AV block, at the time of the syncope, this is very useful. Premonitory symptoms (Nausea, pallor, diaphoresis, flushing), or triggers (Valsalva, Pain, Emotion, Prolonged Standing, Dehydration) are very useful in making the diagnosis. Vasovagal syncope is generally benign.

These premonitory symptoms were negative predictors of adverse outcomes in EGSYS.

Summary:in patients who truly have syncope as the chief complaint (It's not seizure, and it's not abdominal pain, chest pain, hypotension, dyspnea, headache, and VS and rhythm are normal in the ED), and after
ruling out the bleeding, stroke, and obstructive problems, we’re left with
these worrisome predictors:

--Admit for observation patients with presence of 1-2 or more high risk factor (in case of pre-syncope or near syncope, which is much lower risk than full syncope, more than one high risk factor is usually required)--Ideally, all of these predictors would be studied with multivariate analysis to find if any are covariate. Until then, I consider any of these to be independent adverse risk factors.

initial evaluation in patients referred urgently to general hospital: the EGSYS

score. Heart 2008;94(12):1620–6.

Score interpretation: At 2 years, patients with a score of greater than or equal to 3 had mortality of 17% and 21% in the derivation and validation groups, vs. 3% and 2% for those with a score less than 3.

Background: Syncopal episodes are common among older adults; etiologies range from benign to life-threatening. We determined the frequency, yield, and costs of tests obtained to evaluate older persons with syncope. We also calculated the cost per test yield and determined whether the San Francisco Syncope Rule (SFSR) improved test yield.Methods: Review of 2,106 consecutive patients 65 years and older admitted following a syncopal episode.Results: Electrocardiograms (99%), telemetry (95%), cardiac enzymes (95%), and head computed tomography (CT) (63%) were the most frequently obtained tests. Cardiac enzymes, CTs, echocardiograms, carotid ultrasounds, and electroencephalography all affected diagnosis or management in <5 2="" and="" b="" cases="" determine="" etiology="" helped="" of="" syncope="" the="" time.=""> Postural blood pressure, performed in only 38% of episodes, had the highest yield with respect to affecting diagnosis (18-26%) or management (25-30%) and determining etiology of the syncopal episode (15-21%).5>

The cost per test affecting diagnosis or management was highest for electroencephalography ($32,973), CT ($24,881), and cardiac enzymes ($22,397) and lowest for postural blood pressure ($17-$20). The yields and costs for cardiac tests were better among patients meeting, than not meeting, SFSR. For example, the cost per cardiac enzymes affecting diagnosis or management was $10,331 in those meeting, versus $111,518 in those not meeting, the SFSR.Conclusions: Many unnecessary tests are obtained to evaluate syncope. Selecting tests based on history and examination and prioritizing less expensive and higher yield tests would ensure a more informed and cost-effective approach to evaluating older patients with syncope.

Objectives: The aim of this study was to
develop and validate a clinicaldecision rule (CDR) to predict
1-month serious outcome and all-causedeath in patients presenting
with syncope to the emergency department.

Background: Syncope is a
common, potentially serious condition accountingfor many hospital
admissions. Methods: This was a single
center, prospective, observational study ofadults presenting to the
emergency department with syncope.A CDR was devised from 550
patients in a derivation cohort andtested in a validation cohort of
a further 550 patients. Results:
One-month serious outcome or all-cause death occurred in 40(7.3%)
patients in the derivation cohort. Independent predictorswere brain natriuretic peptide
concentration greater than 300 pg/ml (oddsratio
[OR]: 7.3), positive fecal occult
blood (OR: 13.2), hemoglobin less than90 g/l (OR: 6.7), oxygen saturation less than94% (OR: 3.0), and Q-waveon the presenting
electrocardiogram (OR: 2.8). One-month seriousoutcome or
all-cause death occurred in 39 (7.1%) patients inthe validation
cohort. The ROSE (Risk stratification Of Syncopein the Emergency
department) rule had a sensitivity
and specificityof 87.2% and 65.5%, respectively, and a
negative predictivevalue of 98.5%. An elevated B-type natriuretic
peptide (BNP)concentration alone was a major predictor of serious
cardiovascularoutcomes (8 of 22 events, 36%) and all-cause deaths
(8 of 9deaths, 89%).
Conclusions: The ROSE rule has excellent sensitivity and negative
predictivevalue in the identification of high-risk patients with
syncope.As a component, BNP seems to be a major predictor of
seriouscardiovascular outcomes and all-cause death. The ROSE rule
andBNP measurement might be valuable risk stratification toolsin patients with emergency presentations of syncope and shouldnow
be subjected to external validation.

Study objective: We identify predictors of 30-day serious events after
syncope in older adults. Methods: We
reviewed
the medical records of older adults (age ≥60 years) who presented with syncope
or near syncope to one of 3 emergency departments (EDs) between 2002 and 2005.
Our primary outcome was occurrence of a predefined serious event within 30 days
after ED evaluation. We used multivariable logistic regression to identify
predictors of 30-day serious events. Results:
Of 3,727 potentially eligible patients, 2,871 (77%) met all eligibility
criteria. We excluded an additional 287 patients who received a diagnosis of a
serious clinical condition while in the ED. In the final study cohort
(n=2,584), we identified 173 (7%) patients who experienced a 30-day serious
event. High-risk predictors included age
greater than 90 years, male sex, history of an arrhythmia, triage systolic
blood pressure greater than 160 mm Hg, abnormal ECG result, and abnormal
troponin I level. A low-risk predictor was a complaint of near syncope rather than
syncope. A risk score, generated by summing high-risk predictors and
subtracting the low-risk predictor, can stratify patients into low- (event rate
2.5%; 95% confidence interval [CI] 1.4% to 3.6%), intermediate- (event rate
6.3%; 95% CI 5.1% to 7.5%), and high-risk (event rate 20%; 95% CI 15% to 25%)
groups. Conclusion: We identified
predictors of 30-day serious events after syncope in adults aged 60 years and
greater. A simple score was able to stratify these patients into distinct risk
groups and, if externally validated, might have the potential to aid ED
decision making.

Syncope is a common reason
for emergency department (ED) visits, and patients are often admitted to
exclude syncope of cardiovascular origin. Population-based data on patterns and
predictors of cardiac outcomes may improve decision-making. Our objective was
to identify patterns and predictors of short-term cardiac outcomes in ED
patients with syncope. Administrative data from an integrated health system of
11 Southern California EDs were used to identify cardiac outcomes after ED
presentation for syncope from January 1, 2002, to December 31, 2005. Syncope
and cause of death were identified by codes from the International Classification
of Disease, Ninth Revision. Cardiac outcomes included cardiac death and
hospitalization or procedure consistent with ischemic heart disease, valvular
disease, or arrhythmia. Predictors of cardiac outcomes were identified through
multivariate logistic regression. There were 35,330 adult subjects who
accounted for 39,943 ED visits for syncope. Risk of cardiac outcome sharply
decreased following the 7 days after syncope. A 7-day cardiac outcome occurred
in 893 cases (3%). Positive predictors of 7-day cardiac outcomes included age greater than 60 years,
male gender, congestive heart failure, ischemic heart disease, cardiac
arrhythmia, and valvular heart disease. Negative predictors included dementia,
pacemaker, coronary revascularization, and cerebrovascular disease.

There was an age-dependent relation between
7-day cardiac outcomes and arrhythmia and valvular disease, with younger
patients ( less than 60 years of age) having greater risk of an event compared
to their same-age counterparts. In conclusion, ED decision-making should focus
on risk of cardiac event in the first 7 days after syncope and special
attention should be given to younger patients with cardiac co-morbidities.

Background Little is known about the epidemiology and prognosisof syncope in the general population.Methods We evaluated the
incidence, specific causes, and prognosisof syncope among women and
men participating in the FraminghamHeart Study from 1971 to 1998.Results Of 7814 study
participants followed for an average of17 years, 822 reported
syncope. The incidence of a first reportof syncope was 6.2 per 1000
person-years. The most frequentlyidentified causes were vasovagal
(21.2 percent), cardiac (9.5percent), and orthostatic (9.4
percent); for 36.6 percent thecause was unknown. The
multivariable-adjusted hazard ratiosamong participants with syncope
from any cause, as comparedwith those who did not have syncope,
were 1.31 (95 percent confidenceinterval, 1.14 to 1.51) for death
from any cause, 1.27 (95 percentconfidence interval, 0.99 to 1.64)
for myocardial infarctionor death from coronary heart disease, and
1.06 (95 percent confidenceinterval, 0.77 to 1.45) for fatal or
nonfatal stroke. The correspondinghazard ratios among participants
with cardiac syncope were 2.01(95 percent confidence interval, 1.48
to 2.73), 2.66 (95 percentconfidence interval, 1.69 to 4.19), and
2.01 (95 percent confidenceinterval, 1.06 to 3.80). Participants
with syncope of unknowncause and those with neurologic syncope had
increased risksof death from any cause, with multivariable-adjusted
hazardratios of 1.32 (95 percent confidence interval, 1.09 to 1.60)and 1.54 (95 percent confidence interval, 1.12 to 2.12), respectively.There was no increased risk of cardiovascular morbidity or mortalityassociated with vasovagal (including orthostatic and medication-related)syncope.Conclusions
Persons with cardiac syncope are at increased riskfor death from
any cause and cardiovascular events, and personswith syncope of
unknown cause are at increased risk for deathfrom any cause.
Vasovagal syncope appears to have a benign prognosis.

AbstractPURPOSE: To determine the diagnostic yield of
a standardized sequential evaluation of patients with syncope in a
primary care teaching hospital. PATIENTS AND METHODS: All
consecutive patients who presented to the emergencydepartment
with syncope as a chief complaint were enrolled. Their evaluation
included initial and routine clinical examination, including carotid sinus
massage, as well as electrocardiography and basic laboratory testing. Targeted
tests, such as echocardiography, were used when a specific entity was suspected
clinically. Other cardiovascular tests (24-hour Holter monitoring, ambulatory
loop recorder ECG, upright tilt test, and signal-averaged electrocardiography)
were performed in patients with unexplained syncope after the initial
steps. Electrophysiologic studies were performed in selected patients only as
clinically appropriate. Follow-up information on recurrence and mortality were
obtained every 6 months for as long as 18 months for 94% (n = 611) of the
patients. RESULTS: After the initial clinical evaluation, a suspected
cause of syncope was found in 69% (n = 446) of the 650 patients,
including neurocardiogenic syncope (n = 234, 36%), orthostatic hypotension
(n = 156, 24%), arrhythmia (n = 24, 4%), and other diseases (n = 32, 5%). Of
the 67 patients who underwent targeted tests, suspected diagnoses were
confirmed in 49 (73%) patients: aortic stenosis (n = 8, 1%), pulmonary embolism
(n = 8, 1%), seizures/stroke (n = 30, 5%), and other diseases (n = 3).
Extensive cardiovascular workups, which were performed in 122 of the 155
patients in whom syncope remained unexplained after clinical assessment,
provided a suspected cause of syncope in only 30 (25%) patients,
including arrhythmias in 18 (60%), all of whom had abnormal baseline ECGs. The
18-month mortality was 9% (n = 55, including 8 patients with sudden death); syncope
recurred in 15% (n = 95) of the patients. CONCLUSION: The diagnostic
yield of a standardized clinical evaluation of syncope was 76%, greater
than reported previously in unselected patients. Electrocardiogram-based risk
stratification was useful in guiding the use of specialized cardiovascular
tests.

Objectives: To develop and validate a risk score predictingarrhythmias
for patients with syncope remaining unexplainedafter emergency
department (ED) noninvasive evaluation. Methods:One cohort
of 175 patients with unexplained syncope (Geneva,Switzerland) was
used to develop and cross-validate the riskscore; a second cohort
of 269 similar patients (Pittsburgh,PA) was used to validate the
system. Arrhythmias as a causeof syncope were diagnosed by cardiac
monitoring or electrophysiologictesting. Data from the patient's
history and 12-lead emergencyelectrocardiography (ECG) were used to
identify predictors ofarrhythmias. Logistic regression was used to
identify predictorsfor the risk-score system. Risk-score
performance was measuredby comparing the proportions of patients
with arrhythmias atvarious levels of the score and receiver
operating characteristic(ROC) curves. Results: The
prevalence of arrhythmic syncopewas 17% in the derivation cohort
and 18% in the validation cohort.Predictors of arrhythmias were
abnormal ECG (odds ratio [OR]:8.1, 95% confidence interval [CI] =
3.0 to 22.7), a historyof congestive heart failure (OR: 5.3, 95% CI
= 1.9 to 15.0),and age older than 65 (OR: 5.4, 95% CI = 1.1 to
26.0). In thederivation cohort, the risk of arrhythmias ranged from
0% (95%CI = 0 to 6) in patients with no risk factors to 6% (95% CI= 1 to 15) for patients with one risk factor, 41% (95% CI =26
to 57) for patients with two risk factors, and 60% (95% CI= 32 to
84) for those with three risk factors. In the validationcohort,
these proportions varied from 2% (95% CI = 0 to 7) withno risk
factors to 17% (95% CI = 10 to 27) with one risk factor,35% (95% CI
= 24 to 46) with two risk factors, and 27% (95%CI = 6 to 61) with
three risk factors. Areas under the ROC curvesranged from 0.88 (95%
CI = 0.84 to 0.91) for the derivationcohort to 0.84 (95% CI = 0.77
to 0.91) after cross-validationwithin the same cohort and 0.75 (95%
CI = 0.68 to 0.81) forthe external validation cohort. Conclusions:
In patients withunexplained syncope, a risk score based on clinical
and ECGfactors available in the ED identifies patients at risk forarrhythmias. Key words: unexplained syncope; arrhythmia; risk factor;
scoring system

AbstractBACKGROUND: In some patients with syncope
health care is inappropriate and ineffective. In a recent observational
investigation in community hospitals of the Lazio region of Italy (the
OESIL study) 54.4% of patients admitted with syncope from the emergency
room were discharged without a conclusive diagnosis. AIM OF THE STUDY: A
simplified two-step diagnostic algorithm was developed and prospectively implemented
in nine community hospitals of the Lazio region of Italy in order to
improve the diagnostic performance of clinicians, thereby reducing the number
of undiagnosed patients. STUDY POPULATION: The study population included
195 consecutive patients (85 males and 110 females, mean age 62.5 years, range
13-95 years) presenting with a syncopal spell at the emergency room of
one of the nine participating hospitals in a 2-month period. RESULTS:
The systematic implementation of the proposed diagnostic algorithm resulted in
a striking reduction of undiagnosed cases. The percentage of patients
discharged without a conclusive diagnosis decreased from 54.4% to 17.5%.
Neurally mediated syncope was diagnosed in 35.2% of cases, cardiac syncope
in 20.9% and neurological syncope in 13.8%. CONCLUSIONS: The use
of specific, simplified diagnostic guidelines and algorithms results in an
improvement of overall clinical performance. However, the development of such
decision-making aids should carefully consider the local circumstances of daily
clinical practice. Copyright 2000 The European Society of Cardiology.

AIMS: Aim of the present study was the development and the
subsequent validation of a simple risk classification system for patients
presenting with syncope to the emergency departments. METHODS AND RESULTS:
A group of 270 consecutive patients (145 females, mean age 59.5 years)
presenting with syncope to the emergency departments of six community hospitals
of the Lazio region of Italy was used as a derivation cohort for the
development of the risk classification system. Data from the baseline clinical
history, physical examination and electrocardiogram were used to identify
independent predictors of total mortality within the first 12 months after the
initial evaluation. Multivariate analysis allowed the recognition of the
following predictors of mortality: (1) age greater than 65 years; (2) cardiovascular
disease in clinical history; (3) syncope without prodromes; and (4) abnormal
electrocardiogram. The OESIL (Osservatorio Epidemiologico sulla Sincope nel
Lazio) score was calculated by the simple arithmetic sum of the number of
predictors present in every single patient. Mortality increased significantly
as the score increased in the derivation cohort (0% for a score of 0, 0.8% for
1 point; 19.6% for 2 points; 34.7% for 3 points; 57.1% for 4 points;
p less than 0,0001 for trend). A similar pattern of increasing mortality with
increasing score was prospectively confirmed in a second validation cohort of
328 consecutive patients (178 females; mean age, 57.5 years). CONCLUSIONS:
Clinical and electrocardiographic data available at presentation to the
emergency department can be used for the risk stratification of patients with
syncope. The OESIL risk score may represent a simple prognostication tool that
could be usefully employed for the triage and management of patients with
syncope in emergency departments.

Electrocardiographic recordings were evaluated by
the emergency physician and subsequently reviewed
by a cardiologist, only in case of a specific
request. The tracings were considered abnormal in
the following cases:
1. Rhythm abnormalities (atrial fibrillation or
flutter, supraventricular tachycardia, multifocal
atrial tachycardia, frequent or repetitive
premature supraventricular or ventricular complexes,
sustained or non-sustained ventricular
tachycardia, paced rhythms),
2. Atrioventricular or intraventricular conduction
disorders (complete atrioventricular block,
Mobitz I or Mobitz II atrioventricular block,
bundle branch block or intraventricular conduction
delay),
3. Left or right ventricular hypertrophy,
4. Left axis deviation,
5. Old myocardial infarction,
6. ST segment and T wave abnormalities consistent
with or possibly related to myocardial
ischemia.

San Francisco rule:
patients greater than age 75, anabnormal (ECG), hematocrit less than or equal to 30,a complaint of SOB, BP less than 90, or a history of
CHF,was 96% sensitive (95% CI 92-100) and 62% specific (95% CI58-62).

Objective: The causes of syncope are usually benign, but areoccasionally associated with significant morbidity and mortality.This
study compares a clinical decision rule and physician judgmentwhen
predicting serious outcomes in patients with syncope. Methods:In
a prospective cohort study, attending emergency physiciansevaluated
patients presenting to a university teaching hospitalwith syncope
or near syncope. When possible a second physicianalso evaluated
patients. As part of their evaluation, physicianswere asked to
predict the chance (0–100%) of the patientdeveloping a predefined
serious outcome. All patients were followedto determine whether
they had suffered a serious outcome withinseven days of their ED
visit. Analyses included sensitivityand specificity for a low risk
judgment threshold, and comparisonof areas under the receiver
operating characteristic curve (ROC)with 95% confidence intervals.
Kappa coefficients were usedto measure observer agreement. Results:
During the 20-monthstudy there were 684 visits for syncope, 79
resulting in seriousoutcomes. Of the patients to whom the
physicians assigned aprobability of serious outcome of 2% or less,
5 went on to developserious outcomes. The sensitivity of this low
risk 2% thresholdwas 94% (95%CI 86%–98%), with a specificity of 41%
(95%CI40%–42%). Agreement for this determination of risk wasonly
fair, kappa = 0.44 (95%CI 0.34–0.54). The SFSR predictedthe 5
patients with serious outcomes classified as low riskby physician
judgment and had good overall sensitivity 96% (95%CI92%–100%) and
specificity 62% (95%CI 58%–66%). Thearea under the ROC was 0.90
(95%CI 0.86–0.94) for theSFSR and was significantly better (p =
0.01) than physicianjudgment 0.82 (95%CI 0.77–0.88). Conclusions:
The SFSRperformed better than physician judgment when predicting
whichpatients with syncope will develop serious outcomes. This
suggestsgreat potential for the rule to help with physician
decisionmaking.

Methods In a prospective cohort study, consecutive patients with syncope or near syncope presenting to an emergency department (ED) of a teaching hospital were identified and enrolled from July 15, 2002, to August 31, 2004. Patients with trauma, alcohol, or drug-associated loss of consciousness and definite seizures were excluded. Physicians prospectively applied the San Francisco Syncope Rule after their evaluation, and patients were followed up to determine whether they had had a predefined serious outcome within 30 days of their ED visit.

Results: Seven hundred ninety-one consecutive visits were evaluated for syncope, representing 1.2% of all ED visits. The average age was 61 years, 54% of patients were women, and 59% of patients were admitted. Fifty-three visits (6.7%) resulted in patients having serious outcomes that were undeclared during their ED visit. The rule was 98% sensitive (95% confidence interval [CI] 89% to 100%) and 56% specific (95% CI 52% to 60%) to predict these events. In this cohort, the San Francisco Syncope Rule classified 52% of the patients as high risk, potentially decreasing overall admissions by 7%. If the rule had been applied only to the 453 patients admitted, it might have decreased admissions by 24%.

Conclusion: The San Francisco Syncope Rule performed with high sensitivity and specificity in this validation cohort and is a valuable tool to help risk stratify patients. It may help with physician decisionmaking and improve the use of hospital admission for syncope.

14) External Validation of the San Francisco Syncope Rule
in the Canadian Setting. [Ann Emerg
Med. 2010;55:464-472.

External Validation much less sensitive and specific: 90% and 33%

Study objective: Syncope is
a common disposition challenge for emergency physicians. Among the risk
stratification. instruments available,
only the San Francisco Syncope Rule is rigorously developed. We evaluate its
performance in Canadian emergency department (ED) syncope patients. Methods:
This retrospective review included
patients aged 16 years or older who fulfilled the definition of syncope
(transient loss of consciousness with complete recovery) and presented to a
tertiary care ED during an 18-month period. We excluded patients with ongoing
altered mental status, alcohol/illicit drug use, seizure, and head and severe
trauma. Patient characteristics,5 predictors for the rule (history of
congestive heart failure, hematocrit level less than 30%, abnormal ECG characteristics,
shortness of breath, and triage systolic blood pressure less than 90 mm Hg), and
outcomes (as per the original study) were extracted. Results: Of 915 visits
screened, 505 were included. Forty-nine (9.7%) visits were associated with
serious outcomes. The rule performed with a sensitivity of 90% (44/49 outcomes;
95% confidence interval [CI] 79% to 96%) and a specificity of 33% (95% CI 32%
to 34%). Including monitor abnormalities in the ECG variable would improve
sensitivity to 96% (47/49 outcomes; 95% CI 87% to 99%). Although physicians
failed to predict 2 deaths, the rule would have predicted all 3 deaths that
occurred after ED discharge. Implementing th e rule in our setting would
increase the admission rate from 12.3% to 69.5%. Conclusion: In this
retrospective Canadian study, the San Francisco Syncope Rule performed with
comparable sensitivity but significantly poorer specificity than previously
reported. Implementing the rule would significantly increase admission rates.
Further studies to either refine the San Francisco Syncope Rule or develop a
new rule are needed. [Ann Emerg Med. 2010;55:464-472.]

b. Long-term severe outcomes were 9.3% (40 deaths, 6.0%;
22 major therapeutic procedures, 3.3%), and their occurrence was correlated
with an age _65 years, history of neoplasms, cerebrovascular diseases, structural
heart diseases, and ventricular arrhythmias.

AbstractPURPOSE: To review the literature on
diagnostic testing in syncope and provide recommendations for a
comprehensive, cost-effective approach to establishing its cause. DATA
SOURCES: Studies were identified through a MEDLINE search (1980 to present)
and a manual review of bibliographies of identified articles. STUDY
SELECTION: Papers were eligible if they addressed diagnostic testing in syncope
or near syncope and reported results for at least 10 patients. DATA
EXTRACTION: The usefulness of tests was assessed by calculating diagnostic
yield: the number of patients with diagnostically positive test results divided
by the number of patients tested or, in the case of monitoring studies, the sum
of true-positive and true-negative test results divided by the number of
patients tested. DATA SYNTHESIS: Despite the absence of a diagnostic
gold standard and the paucity of data from randomized trials, several points
emerge. First, history, physical examination, and electrocardiography are the
core of the syncope workup (combined diagnostic yield, 50%).
Second, neurologic testing is rarely helpful unless additional neurologic signs
or symptoms are present (diagnostic yield of electroencephalography, computed
tomography, and Doppler ultrasonography, 2% to 6%). Third, patients in whom
heart disease is known or suspected or those with exertional syncope are
at higher risk for adverse outcomes and should have cardiac testing, including
echocardiography, stress testing. Holter monitoring, or intracardiac
electrophysiologic studies, alone or in combination (diagnostic yields, 5% to
35%). Fourth, syncope in the elderly often results from polypharmacy and
abnormal physiologic responses to daily events. Fifth, long-term loop
electrocardiography (diagnostic yield, 25% to 35%) and tilt testing (diagnostic
yield less than or greater than 60%) are most useful in patients with recurrent syncope
in whom heart disease is not suspected. Sixth, psychiatric evaluation
can detect mental disorders associated with syncope in up to 25% of
cases. Seventh, hospitalization may be indicated for patients at high risk for
cardiac syncope (those with an abnormal electrocardiogram, organic heart
disease, chest pain, history of arrhythmia, age > 70 years) or with acute
neurologic signs. CONCLUSIONS: Many tests for syncope have a low
diagnostic yield. A careful history, physical examination, and
electrocardiography will provide a diagnosis or determine whether diagnostic
testing is necessary in most patients. [References: 34]

Background—The primary aim and central hypothesis of the study are that a designated syncope unit in the emergency department improves diagnostic yield and reduces hospital admission for patients with syncope who are at intermediate risk for an adverse cardiovascular outcome. Methods and Results—In this prospective, randomized, single-center study, patients were randomly allocated to 2 treatment arms: syncope unit evaluation and standard care. The 2 groups were compared with 2 test for independence of categorical variables. Wilcoxon rank sum test was used for continuous variables. Survival was estimated with the Kaplan-Meier method. One hundred three consecutive patients (53 women; mean age 64 17 years) entered the study. Fifty-one patients were randomized to the syncope unit. For the syncope unit and standard care patients, the presumptive diagnosis was established in 34 (67%) and 5 (10%) patients (P less than 0.001), respectively, hospital admission was required for 22 (43%) and 51 (98%) patients (P less than 0.001), and total patient-hospital days were reduced from 140 to 64. Actuarial survival was 97% and 90% (P = 0.30), and survival free from recurrent syncope was 88% and 89% (P = 0.72) at 2 years for the syncope unit and standard care groups, respectively. Conclusions—The novel syncope unit designed for this study significantly improved diagnostic yield in the emergency department and reduced hospital admission and total length of hospital stay without affecting recurrent syncope andvall-cause mortality among intermediate-risk patients. Observations from the present study provide benchmark data for improving patient care and effectively utilizing healthcare resources.

18) Venkatesh Thiruganasambandamoorthy et al. Outcomes in Presyncope Patients: A Prospective Cohort Study. Annals of Emergency Medicine March 2015; Volume 65, Issue 3, Pages 268–276.e6By 30 days, 2 of 881 patients had died, but it was not know if these were from cardiovascular causes. This is substantially less that the mortality rate for syncope. 5% had "serious outcomes," but because of poor definitions, this article greatly exaggerates the danger.

Study objective: Presyncope is the sudden onset of a sense of impending loss of consciousness without losing consciousness (which differentiates it from syncope). Our goals are to determine the frequency of emergency department (ED) presyncope visits, management, 30-day outcomes, and emergency physicians’ outcome prediction.

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